Coadministration of the Vasopressin-2 Receptor Antagonist Tolvaptan and B-Type Natriuretic Peptide Enhances Water and Sodium Excretion without Adversely Affecting Renal or Neurohumoral Function in Experimental Congestive Heart Failure

Renal responses to atrial natriuretic peptide were examined in conscious dogs with congestive heart failure (tricuspid insufficiency) and in conscious rats with nephrotic syndrome (adriamycin). Heart-failure dogs displayed elevated atrial pressure and heart weights, blunted natriuresis to a saline load, and ascites. Nephrotic rats displayed proteinuria, hypoproteinemia, sodium retention, and ascites. In control animals, atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion. Although atrial natriuretic peptide increased absolute and fractional urine flow rate and urinary sodium excretion in conscious heart-failure dogs and nephrotic rats, the responses were markedly blunted. In heart-failure dogs, infusion of atrial natriuretic peptide increased plasma concentrations of norepinephrine and epinephrine. In nephrotic rats, renal denervation reversed the blunted diuretic and natriuretic responses to atrial natriuretic peptide. Mean arterial pressure, glomerular filtration rate, and p-aminohippurate clearance were affected similarly by atrial natriuretic peptide in heart-failure dogs or nephrotic rats vs. control animals. Conscious congestive heart-failure dogs and conscious nephrotic rats have blunted diuretic and natriuretic responses to atrial natriuretic peptide.

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Co-Targeting of the V2 Receptor with Tolvaptan and the Natriuretic Peptide A-Receptor with B-Type Natriuretic Peptide Enhances Water and Sodium Excretion without Adversely Affecting Renal Function: A Novel Physiologic Approach to Sodium and Water Retention in Experimental Heart Failure

Journal of Cardiac Failure ◽

10.1016/j.cardfail.2006.06.287 ◽

2006 ◽

Vol 12 (6) ◽

pp. S84-S85 ◽

Cited By ~ 1

Author(s):

Lisa C. Costello-Boerrigter ◽

Guido Boerrigter ◽

Gail J. Harty ◽

John C. Burnett

Keyword(s):

Heart Failure ◽

Renal Function ◽

Natriuretic Peptide ◽

Sodium Excretion ◽

Water Retention ◽

Experimental Heart Failure ◽

V2 Receptor ◽

Water And Sodium Excretion

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Role of endogenous atrial natriuretic peptide in congestive heart failure

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1989.257.3.r641 ◽

1989 ◽

Vol 257 (3) ◽

pp. R641-R646 ◽

Cited By ~ 1

Author(s):

M. Awazu ◽

T. Imada ◽

V. Kon ◽

T. Inagami ◽

I. Ichikawa

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Glomerular Filtration Rate ◽

Atrial Natriuretic Peptide ◽

Glomerular Filtration ◽

Natriuretic Peptide ◽

Sodium Excretion ◽

Filtration Rate ◽

Retention Characteristic ◽

Atrial Natriuretic

Effects of purified rabbit anti-rat 25-amino acid atrial natriuretic peptide (ANP) immunoglobulin G (IgG) on renal sodium excretion and glomerular filtration rate were studied in a rat model of congestive heart failure (CHF) having high circulating ANP levels. Bolus injection of anti-ANP into anesthetized rats with surgically induced myocardial infarction (MI) significantly and markedly depressed both absolute and fractional urinary excretion of sodium without affecting mean arterial pressure or glomerular filtration rate. By contrast, anti-ANP failed to affect these renal functions in normal or acutely water-deprived rats. Nonimmune IgG did not affect renal function in MI rats. These results indicate that high circulating ANP plays an important role in sodium homeostasis of congestive heart failure: by promoting sodium excretion, ANP opposes the tendency of sodium retention characteristic of CHF.

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